Abstract
Takayasu's arteritis (TAK) is a rare chronic arteritis that can lead to serious consequences. Understanding of the pathogenesis of TAK remains limited, and effective therapeutic strategies for this condition are lacking. Previous studies have suggested that there may be an association between TAK and the interaction between Mycobacterium tuberculosis infection and genetic susceptibility. Emerging data indicate that the nucleotide-binding and oligomerization domain (NOD)-like receptor pyrin domain-containing protein 3 receptor (NLRP3) inflammasome may be involved in the pathogenesis of TAK, potentially contributing to the initiation of the disease. This review summarizes the current epidemiological data, possible mechanisms, and targeting strategies of TAK, focusing on the involvement of the NLRP3 inflammasome in the pathogenesis of TAK, and provides new insights into the prevention and treatment of this condition.